1. Traumatic brain injury
Dr. Syed Faheem Shams
MD (Part III) student
Dept. of Psychiatry
BSMMU

2. Objectives
Traumatic brain injury-
What? Epidemiology? Cause and
effect?
Types? When to give attention?
Why we need to know?

3. Brain InjuriesBrain Injuries
Congenital brain injury
Pre-birth During birth
Acquired Brain Injury
After birth process
Traumatic Brain Injury
(external physical force)
Non-traumatic
Brain Injury
Closed Head
Injury
Open Head
Injury

4. What is a TBI?What is a TBI?
Sudden damage to the brain due to anSudden damage to the brain due to an
external forceexternal force

5. Two types of TBITwo types of TBI
OPEN-HEAD INJURY
(penetrating)
Example:
• Skull fracture that
penetrates the brain
• Gunshot wound
CLOSED-HEAD INJURY
(non penetrating)
when the head forcefullywhen the head forcefully
collides with anothercollides with another
objectobject
Example:
• Coup-Contra Coup
• Diffuse axonal injury

6. ICD-10 S 06- Intracranial injury
S06.0 Concussion
Commotio cerebri
S06.1 Traumatic cerebral oedema
S06.2 Diffuse brain injury
Cerebral
contusion NOS
laceration NOS
Traumatic compression of brain NOS
S06.3 Focal brain injury
Focal:
cerebral:
contusion
laceration
traumatic intracerebral haemorrhage
S06.4 Epidural haemorrhage
Extradural haemorrhage (traumatic)
S06.5 Traumatic subdural haemorrhage
S06.6 Traumatic subarachnoid haemorrhage
S06.7 Intracranial injury with prolonged coma
S06.8 Other intracranial injuries
Traumatic haemorrhage:
cerebellar
intracranial NOS
S06.9 Intracranial injury, unspecified
Brain injury NOS

7. Brain Injury Facts
Worldwide
• Brain injury is the leading cause of death
and disability
• Traumatic brain injury is the leading cause
of seizure disorders
• The global incidence rate of TBI is
estimated at 200/100 000 people per year
http://www.internationalbrain.org/?q=brain-injury-facts
http://injuryprevention.bmj.com/content/16/Suppl_1/A17.2.abstract

8. Brain Injury Facts
(contd.)
United States Europe
01 million hospital
admissions per year
In the south of Europe, the
main cause --traffic
accidents
In the north of Europe, the
major causes- falls,
mainly related to alcohol
use (
Tagliaferri et al 2006)
http://injuryprevention.bmj.com/content/16/Suppl_1/A17.2.abstract
01 million Treated and
released
from hospital
80,000 Some TBI-
related
disability
50,000 die
Males>
females
15-24 years

9. EpidemiologyEpidemiology
Percentage of Average Annual TBI-related emergency department visits,Percentage of Average Annual TBI-related emergency department visits,
hospitalizations, and deaths, by External Cause, United States, 1995-2001hospitalizations, and deaths, by External Cause, United States, 1995-2001
Falls, 28%
Motor Vehicle-
Traffic, 20%
Struck
By/Against, 19%
Assault, 11%
Unknown,
9%
Other, 7%
Pedal Cycle
(non MV), 3%
Suicide, 1%
Other Transport,
2%

10. The greatest number of TBIs occur in people aged
15–24
TBI rates are higher in males
Occupational Therapy and Physical Dysfunction: Principles, Skills and Practice.
Edinburgh: Churchill Livingstone. pp. 395–96

11. TBI in children can beTBI in children can be
especially devastatingespecially devastating

12. Brain Rates of DevelopmentBrain Rates of Development
P-O
C
T
F-T
P-O
C
F-T P-O
T
C
F-T
5 Distinct
Periods of
Maturation
P - O parietal/
occipital
C central
(limbic &
brainstem)
T temporal
F - T frontal/
temporal

13. Severity of traumatic brain
injury
GCS PTA LOC
Mild 13-15 <1 day 0-30 min
Moderate 9-12 >1- 14 days >30 min–
6 hrs
Severe 3-8 >14 days >6 hrs
Lishman’s Organic psychiatry, 4th
edition

14. In severe diffuse traumatic injury:
PTA (weeks) = 0.4 × LOC (days) + 3.6
Katz and Alexander (1994)

15. Brain ConcussionBrain Concussion
• Impaired function
• No structural damage
• Extreme variance in severity
– LOC
• Diffuse

16. CONCUSSION vs CONTUSION
CONCUSSION
• Temporary loss of
neurologic function
with no structural
damage lasting for a
few seconds to few
minutes
CONTUSION
• More severe injury in
which the brain is
bruised, with possible
surface hemorrhage
• Unconscious for more
than a few seconds or
minutes
• Picture is somewhat
similar to that of
shock

17. Coup Contra-Coup InjuryCoup Contra-Coup Injury

18. Epidural haemorrhage Subdural haemorrhage

19. Subarachnoid haemorrhage

20. ManagementManagement
The acute management of severeThe acute management of severe
traumatic brain injury:traumatic brain injury:
– 1. Protect the airway & oxygenation
– 2. Ventilate to normocapnia
– 3. Correct hypovolaemia & hypotension
– 4. CT Scan when appropriate
– 5. Neurosurgery if indicated
– 6. Intensive Care for further monitoring and
management

21. Significant Head InjuriesSignificant Head Injuries
Signs of increased ICP---Signs of increased ICP---
–Visual difficultiesVisual difficulties
–VomitingVomiting
–DyspneaDyspnea
– BradycardiaBradycardia

22. How Brain Injuries treated?How Brain Injuries treated?

23. Interesting findings
The most common areas to have focal
lesions in non-penetrating traumatic brain
injury are the orbitofrontal cortex and the
anterior temporal lobes
"Frontal lobe dysfunction following closed head injury. A review of the literature". Journal of Nervous & Mental
Disorders 178 (5): 282–291. "Deformation of the human brain induced by mild acceleration". Journal of
Neurotrauma 22 (8): 845–856.
"Frontal-subcortical circuits and human behavior".Archives of Neurology 50 (8): 873–880.
"TASIT: A new clinical tool for assessing social perception after traumatic brain injury". Journal of Head Trauma
Rehabilitation 18 (3): 219–238.

24. Interesting findings (contd.)
• Alexithymia, a deficiency in identifying,
understanding, processing, and describing
emotions occurs in 60.9% of individuals
with TBI
Alexithymia and emotional empathy following traumatic brain injury". J Clin Exp
Neuropsychol 32 (3): 259–67.

25. Is head injury a risk for
dementia??
β-amyloid protein have been found to
accumulate in about 30% of patients after
TBI and may form plaques
(Roberts et al. 1994; Ikonomovic et al. 2004)
However, some groups have failed to find
elevated Aβ after head injury
(Adle-Biassette et al. 1996; Macfarlane et al. 1999)

26. PSYCHIATRIC
PROBLEMS
IN
TBI?

27. Adolf Meyer published comprehensive
case reports about patients who
presented behavior disturbances after
head injuries and proposed a set of
disorders called “traumatic insanities”,
which included consciousness alterations,
psychosis, and neurological symptoms (
Neylan 2000)

28. Post-traumatic delirium (post-traumatic
confusional state) and post-traumatic
amnesia
Post-traumatic delirium (confusional state)
shows much variation, depending on the
severity of the injury and its complications

29. Post-traumatic delirium
Apathetic Restless, Irritability Florid delirious states
Withdrawal
Fear, persecutory beliefs, and perplexity are common
Disorientation for time and place is marked at first

30. Post-traumatic delirium (contd.)
As the confusional state improves,
confabulations come to dominate, almost
always accompanied by lack of insight and
disorientation
Associated with misinterpretation of
surroundings and misidentification of people. It
is not unusual for patients to believe that staff or
other patients on the ward are familiar to them
Hallucinatory experiences may be troublesome;
visual hallucinations are most evident

31. Post-traumatic agitation
Patient may be abusive, aggressive,
sexually disinhibited
Occurs in about 10% of patients with
severe brain injury (Brooke et al. 1992)
Last a few days
Agitated behavior is associated with
frontotemporal injury and doubles the risk
of later emotional sequelae (van der Naalt et al.
2000).

32. Post-traumatic amnesia
It ends at the time from which the patient
can later give a clear and consecutive
account of what was happening around
him
Period of unconsciousness + Post-
traumatic delirium

33. Post-traumatic amnesia (contd.)
A study of orientation during PTA showed
that the usual sequence of recovery was
for person place time (Levin 1990).

34. Summary of findings for
depression after TBI
Incidence 15.3%–33%
Kim et al 2007
Prevalence 18.5%–61%
Kim et al 2007
Abnormalities on CT
Levin et al 2005
Lower bilateral
hippocampal volume
Jorge et al 2007
Volume reduction of the left
prefrontal grey matter
Jorge et al 2004
Unemployment
Seel et al 2003; Dikmen et al 2004; Jorge et al 2004
Lower economic status;
aggression; anxiety
Dikmen et al 2004

35. Why depression?
Rupture of neural circuits involving the
prefrontal cortex, amygdala,
hippocampus, basal ganglia, and
thalamus may be related to the
development of depression due TBI. (
Jorge and Starkstein 2005)
The hippocampus is an anatomic region
vulnerable to TBI (Campbell and MacQueen 2004)

36. Treatment of depression in TBI
Citalopram and sertraline (
Turnes-Stokes and MacWalter 2005).
Citalopram (Rapoport et al 2008).
The use of fluoxetine, paroxetine,
venlafaxin, minalcipran, amitryptiline,
desipramine, bupropio presented
generally positive results (Alderfer et al 2005;
Warden et al 2006).

37. Caution with TCAs
Anticholinergic effects of TCAs can
exacerbate cognitive impairment.

38. Summary of findings for Mania
after TBI
Incidence 9%
Jorge et al 1999
Prevalence 4.2%
van Reekum et al 2000
Higher rates for men
van Reekum et al 1996
Lesions in the temporal basal poles
Jorge et al 1993b; Murai and Fujimoto 2003

39. Treatment of Mania in TBI
Valproic acid and lithium, while case
reports pointed out the usefulness of
quetiapine, carbamazepine, clonidine, and
electroconvulsive therapy
(Warden et al 2006; Oster et al 2007)

40. Summary of findings for
Psychosis after TBI
Incidence 0.1%–9.8%
David and Prince 2007
Prevalence 0.7%
van Reekum et al 2000
Damage in frontal and temporal lobes
Achte 1969; Sachdev et al 2001; Fujii and Ahmed 2002a
Predominance of positive symptoms
Sachdev et al 2001
Persecutory (56%), reference (22%), control
(22%), and grandiosity (20%).
Fujii and Ahmed (2001)

41. Treatment of Psychosis in TBI
Typical antipsychotics have
anticholinergic, hypotensive, or sedative
effects, or a strong dopaminergic
antagonism are potentially able to worsen
the already existent deficits for TBI
survivors.
(Feeney et al 1982; Goldstein 1993)

42. Summary of findings for OCD
after TBI
Prevalence 1.6%–15%
Hibbard et al 1998; Deb et al 1999
Oribitofrontal cortex, cingulate cortex and caudate
nucleus damage
Berthier et al 2001; Bilgic et al 2004; Ogai et al 2005
Obsessive slowness; compulsive exercises
practice; aggression
Berthier et al 2001

43. Summary of findings for PTSD
after TBI
Incidence 11.3%–24%
Bryant and Harvey 1998; Bombardier et al 1999
Prevalence 3%–27.1%
Bryant et al 2000; Glaesser et al 2004
Impaired quality of life and social function; chronic
pain
Bryant et al 1999
Posttraumatic amnesia as a protective factor
Sbordone and Liter 1995; Glaesser et al 2004; Gil et al 2005

44. Summary of findings for
Personality change after TBI
Apathy
Prevalence 34.5% after severe TBI
Pelegrín-Valero et al 2001
Younger age; more severe TBI
Kant et al 1998
Affective lability
Prevalence 5%–32.7%
Zeilig et al 1996; Pelegrín-Valero et al 2001
Frontal lobe damage; aggression; anxiety
Robinson et al 1993
Aggression
Prevalence 16.4%–33.7%
Pelegrín-Valero et al 2001; Tateno et al 2003

45. Predictors of poor outcome
• “ Poor response to psychiatric medications
• “ Failure in behavioral programs requiring
memory and problem-solving
• “ Social network failure: divorce, separation
• Failure at work
• “Persistence of chronic pain and headache
symptoms
• “Lack of support system

46. OUTCOME In Severe Brain
injury
Good recovery 25-30%
Moderate disability 15-20%
Sever disability 15%
Vegetative stat 5%
Death 30-35%

48. Thank you all !!